introduction to the immune system Flashcards

(26 cards)

1
Q

What is Immunology?

A

Immunology is the study of our body’s sytems for preventing and treating diseases.

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2
Q

How is the Immune System organized?

A

Innate Immunity - and a second, more specific defence -

Adaptive Immunity. The adaptive immunity can be humoural (ie. B cells and antibodies) or it can be cellular (ie. T cells). White Blood Cells (WBCs) are key players in the immune system.

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3
Q

what are the components of innate immunity?

A

→physical barriers ( skin, mucosal surfaces)
→chemical barriers ( pH, secreted factors)
→phagocytes (monocytes/granulocytes/neutrophils)
→inflammation
→ acute phase response
→cytokines and chemokines
→complement
→natural killer cells

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4
Q

what is the inflammatory response triggered by?

A

→ the release of pro-inflammatory cytokines and chemokines at the site of infection

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5
Q

what is the purpose of the inflammatory response?

A

→localize and eliminate injurious agents and to remove damages tissue components

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6
Q

what occurs during the inflammatory response?

A

→enhanced permeability and extravasation
→neutrophil recruitment
→enhanced cell adhesion
→ enhanced clotting

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7
Q

what are cytokines and chemokines?

A

glycoprotein hormones that affect the immune response

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8
Q

what do cytokines do?

A

they act to modify the behavior of cells in the immune response
most of them are called interleukins

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9
Q

what do chemokines do?

A

act as chemotactic factors that create concentration gradients which attract or repel certain cell types to a site of infection or production

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10
Q

how do macrophages detect microbes?

A

→Macrophages have phagocytic receptors that bind microbes and their components.

→They detect substances that are usually presented on pathogens (non-self).

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11
Q

what are protein-associated molecular patterns PAMPs and give some examples?

A

→PAMPs are small molecular motifs conserved within a class of microbes.

→ glycans 
→ lipopolysaccharides 
→bacterial flagellin 
→ lipoteichoic acid 
→ peptidoglycan 
→nucleic variants normally associated with viruses, such as double-stranded RNA
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12
Q

what are damage-associated molecular patterns (DAMPs) and give some examples

A

→DAMPs are molecules released by stressed cells undergoing necrosis.

→vary greatly depending on the type of cell and injured tissue.

→Some of these endogenous danger signals are proteins
→ heat-shock proteins and cytokines.

→Non-protein DAMPs include ATP, heparin sulfate and DNA.

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13
Q

what are pattern recognition receptors? (PRR) and what are they encoded by?

A

→host factors that specifically recognize a particular type of PAMP.

→ germ-line encoded.

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14
Q

what are the three types of PRR?

A

EXTRACELLULAR:
→they recognize PAMPs outside of a cell and trigger a coordinated response to the pathogen

INTRACELLULAR (CYTOPLASMIC):
→recognize PAMPs inside a cell and act to coordinate a response to the pathogen

SECRETED:
→act to tag circulation pathogens for elimination

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15
Q

how does interferon work?

A

→A virus infects a cell, which then becomes known as the primary infected cell.

→ virus will multiply inside the cell, and, after the cell dies, it will release the viral progeny.

→as the primary infected cell is dying, it releases interferons.

→interferons are picked up by other healthy cells, and they induce the transcription of >400 antiviral genes.

→ healthy cells in an antiviral state so viruses cannot affect them.

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16
Q

what is the ligand and outcome of lectin receptors?

A

LIGAND: terminal mannose, fucose
OUTCOME: phagocytosis

17
Q

what is the ligand and outcome of scavenger receptors?

A

LIGAND: bacterial cell walls, modified low-density lipoproteins

OUTCOME: phagocytosis

18
Q

what is the ligand and outcome of Toll like receptors?

A

LIGAND: lipopolysaccharides together with CD14 (LPS), lipoproteins, unmethylated CpG, flagellin, dsRNA and ssRNA (in endosomes)

OUTCOME: phagocytosis, inflammation,

19
Q

what is the ligand and outcome of NOD like receptors?

A

LIGAND: peptidoglycan from Gram-positive and negative bacteria, some viral DNA and
RNA

OUTCOME: inflammation, cytokine release (IL-1, IL-8)

20
Q

what is the ligand and outcome of RIG-like receptors?

A

LIGAND: dsRNA and 5’-triphosphate RNA

OUTCOME: type I interferon production

21
Q

what are complement proteins?

A

→A system of secreted proteins made in the liver that recognise PAMPs on the surface of microbes and ‘decorate’ or ‘tag’ them.

→The microbes are then cleared by phagocytosis, “opsonised” (C3 sticks to pathogen membranes) or they have holes punched in them.

22
Q

what are the three pathways of activating complement proteins?

A

→recognition of LPS and other PAMPs by the C1q component of the ‘classical’ pathway

→ non-host glycosylation is recognised by MBP (mannan/mannose-binding protein) and other lectins to activate the ‘lectin’ pathway

→ membranes that are recognised as “non-self” activate the ‘alternative’ pathway Complement activation involves a proteolytic cascade.

23
Q

what is the structure of natural killer cells?

A

→they are large granular lymphocytes.

→they make up about 4% of WBCs.

→ lymphocyte-like, but larger with a granular cytoplasm.

→ kill certain tumour cells and virally-infected cells.

→ Target cell destruction is caused by the cytotoxic molecules called granzymes and perforins.

24
Q

how are natural killer cells activated?

A

→Natural killer (NK) cells are activated by loss-of-self.

→An NK cell has an MHC receptor on its surface.

→With an uninfected cell, it will present the ligand for the MHC receptor, stimulating an inhibitory signal that stops the NK cell from killing it.

→ with an infected cell, they do not present this ligand, so the inhibitory signal is not presented

→releases perforin and cytotoxic granules into the infected cell or engages the cell’s death receptors.

25
there are specific diseases associated with innate immunity what are they?
→complement → core defects (eg. C3) linked to the development of autoimmune diseases such as lupus complement → non-core defects linked to susceptibility to specific types of pathogens such as Neisseria (meningitis) macrophage deficiencies → chronic granulomatous disease (CGD); no oxidative burst for bacterial killing macrophage deficiencies → IRF8 (transcription factor) mutations linked to susceptibility to TB → Aicardi-Goutieres syndrome is associated with constitutive production of inflammatory cytokines (defect in regulation of cytokines) → lack of interferon-responsiveness → sensitivity to viral infections (eg. measles)
26
compare the innate and adaptive immune system
→in the innate system, we have macrophages, neutrophils, dendritic cells → in the adaptive system, we have lymphocytes → the innate system acts faster than the adaptive system → the innate system does not hold any 'memory', while the adaptive system does →the innate system is not specific, while the adaptive system is very specific → the innate system has a small number of microbial ligands that are highly conserved between pathogens → the adaptive system has billions of possible antigens →the innate system has germ-line encoded receptors evolved by natural selection which don't change →the adaptive system has receptors that are generated randomly within the individual, they can't be inherited